July 20, 2017

Fighting Ageing with Epitalon

Simple practices can make some difference, such as moderate but regular exercise or calorie restriction, supplementation with antioxidants and healthy living (no alcohol, no smoking, no stress …).

But over the long haul all that really matters is medical biotechnology: progress towards therapies that can repair and reverse the known root causes of aging.

2013 is the year to remember in anti-ageing biotechnology, as it is the first time ever that the age reversing peptide Epitalon was made available to the public.

Your body stopped manufacturing this crucial enzyme since you when were still in your mother’s womb, and from that day on your telomeres have become shorter and shorter … condamning you to a limited lifespan of anywhere from 60 to 120 years.

Telomeres shorten during each cell division, until they become too short for the cell to reproduce, and it brings death or bad mutation to your cells.

The enzyme telomerase allows for replacement of short bits of this DNA known as telomeres, which are otherwise shortened when a cell divides via mitosis.

Only the enzyme telomerase can add DNA sequences to your telomeres to lenghten them, thus allowing more duplication of your cells, adding more years of healthy living to your body.
Unfortunately, taking telomerase by mouth doesn’t work, as it is not able to penetrate the cell from the outside. Only a signal from your pineal gland can trigger the production of telomerase inside the cells. That’s the role of our Epitalon, to send the signal to your cells to start to manufacture telomerase again.

Epitalon is the sole and only product that proved to lenghten human telomeres in published scientific studies. No other product, whatever their advertising tells you, has ever been proven to allow your cells to overcome the Hayflick limit.

Below is an extract of one of the numerous studies that explain and confirm the role of telomeres, and their relation to longevity and health.

Extracts: Telomeres are repeated DNA nucleoprotein structures at the ends of eukaryotic chromosomes (Blackburn, 1991; de Lange, 2005) that protect them from degradation and DNA repair activities, and are essential for chromosomal stability (Chan and Blackburn, 2002).
Telomere repeats can be added de novo by telomerase, a reverse transcriptase that elongates telomeres in cells in which it is expressed (Blackburn, 2005; Flores et al., 2006; Greider, 1998; Greider and Blackburn, 1985; Marion et al., 2009). In telomerase-negative cells, telomeres shorten with each round of cell division as a result of end replication and DNA-degrading activities.
Short telomeres are passed onto daughter cells, and thus telomere shortening is exacerbated by cell division and increasing age in both humans and mice (Flores et al., 2008; Harley et al., 1990).Critically short telomeres can trigger a persistent DNA damage response that leads to cellular senescence and/or apoptosis (Collado et al., 2007; Deng et al., 2008), eventually compromising the regenerative capacity and function of tissues(Blasco, 2007).
Short telomeres are proposed to be suficient to cause the degenerative pathologies associated with aging even in the presence of telomerase activity (Armanios et al., 2009; Hao et al., 2005)

Telomere length measurements in the blood have been shown to be representative of the general health status in humans (Canela et al., 2007; Cawthon et al., 2003; Collerton et al., 2007; Mainous et al., 2010; Valdes et al., 2005) and mice (Bernardes de Jesus et al., 2012), and provide an indicator of the general healthspan.